Assessment of the agreement between wedge hepatic vein pressure and portal vein pressure in cirrhotic patients

2005 ◽  
Vol 37 (8) ◽  
pp. 601-608 ◽  
Author(s):  
U. Thalheimer ◽  
G. Leandro ◽  
D.N. Samonakis ◽  
C.K. Triantos ◽  
D. Patch ◽  
...  
Keyword(s):  
Portal Vein ◽  
Hepatic Vein ◽  
Portal Vein Pressure ◽  
Cirrhotic Patients

scholarly journals Usefulness of portal vein pressure for predicting the effects of tolvaptan in cirrhotic patients

2016 ◽  
Vol 22 (21) ◽  
pp. 5104 ◽  
Author(s):  
Ai Nakagawa ◽  
Masanori Atsukawa ◽  
Akihito Tsubota ◽  
Chisa Kondo ◽  
Tomomi Okubo ◽  
...  
Keyword(s):  
Portal Vein ◽  
Portal Vein Pressure ◽  
Cirrhotic Patients

Plasma insulin, C-peptide, and blood glucose in portal, hepatic and peripheral veins in liver cirrhosis. Effect of intravenous tolbutamide

1981 ◽  
Vol 97 (4) ◽  
pp. 496-502 ◽  
Author(s):  
R. Pelkonen ◽  
H. Kallio ◽  
H. Suoranta ◽  
S.-L. Karonen
Keyword(s):  
Liver Cirrhosis ◽  
Blood Glucose ◽  
Portal Vein ◽  
Hepatic Vein ◽  
Plasma Insulin ◽  
Venous Blood ◽  
Diabetic Patients ◽  
C Peptide ◽  
Control Subjects ◽  
Cirrhotic Patients

Abstract. The responses of portal, hepatic and peripheral venous blood glucose (BG), plasma insulin (IRI) and C-peptide (IRC) levels to iv tolbutamide (200 mg) have been determined in 9 non-diabetic patients with liver cirrhosis and in 6 control subjects. The basal levels of plasma IRI and IRC were similar in patients and controls as were the portal and peripheral BG levels. In the hepatic vein, however, the BG-levels were higher in cirrhotic patients than in controls. After tolbutamide administration the BG-levels were unchanged in the cirrhotic patients but a significant fall in hepatic vein BG was observed in controls. In both groups of subjects the highest post-tolbutamide IRI-levels were found in the portal vein whereas the corresponding IRC-levels were as high in the hepatic as in the portal vein. The increments of portal venous IRI and IRC were signifiantly higher in controls as compared to the cirrhotic patients. Nevertheless, in the peripheral veins the increments of IRI and IRC were very similar in both groups of subjects or even less in the control subjects. The results suggest that in patient with liver cirrhosis the secretion of insulin is not increased but slightly decreased. The production of glucose by the liver also seems to be increased either due to insulin resistance or portal venous shunting of insulin.

Methods for assessing hepatic distending pressure and changes in hepatic capacitance in pigs

2000 ◽  
Vol 279 (4) ◽  
pp. H1796-H1803 ◽  
Author(s):  
Harald Kjekshus ◽  
Cecilie Risoe ◽  
Tim Scholz ◽  
Otto A. Smiseth
Keyword(s):  
Portal Vein ◽  
Blood Volume ◽  
Hepatic Vein ◽  
Close Agreement ◽  
Dynamic Pressure ◽  
Portal Vein Pressure ◽  
Equilibrium Pressure ◽  
Vascular Compliance ◽  
Continuous Measurements ◽  
Valid Method

The equilibrium pressure obtained during simultaneous occlusion of hepatic vascular inflow and outflow was taken as the reference estimate of hepatic vascular distending pressure (Phd). Phdat baseline was 1.1 ± 0.2 (mean ± SE) mmHg higher than hepatic vein pressure (Phv) and 0.7 ± 0.3 mmHg lower than portal vein pressure (Ppv). Norepinephrine (NE) infusion increased Phdby 1.5 ± 0.5 mmHg and Ppvby 3.7 ± 0.6 mmHg but did not significantly increase Phv. Hepatic lobar vein pressure (Phlv) measured by a micromanometer tipped 2-Fr catheter closely resembled Phdboth at baseline and during NE-infusion. Dynamic pressure-volume (PV) curves were constructed from continuous measurements of Phvand hepatic blood volume increases (estimated by sonomicrometry) during brief occlusions of hepatic vascular outflow and compared with static PV curves constructed from Phddeterminations at five different hepatic volumes. Estimates of hepatic vascular compliance and changes in unstressed blood volume from the two methods were in close agreement with hepatic compliance averaging 32 ± 2 ml · mmHg−1· kg liver−1. NE infusion reduced unstressed blood volume by 110 ± 38 ml/kg liver but did not alter compliance. In conclusion, Phlvreflects hepatic distending pressure, and the construction of dynamic PV curves is a fast and valid method for assessing hepatic compliance and changes in unstressed blood volume.

Comparison between portal vein pressure and wedged hepatic vein pressure in hepatitis B-related cirrhosis

1989 ◽  
Vol 9 (3) ◽  
pp. 326-330 ◽  
Author(s):  
Han-Chieh Lin ◽  
Yang-Te Tsai ◽  
Fa-Yauh Lee ◽  
Ting-Tsung Chang ◽  
Sun-Sang Wang ◽  
...  
Keyword(s):  
Hepatitis B ◽  
Portal Vein ◽  
Hepatic Vein ◽  
Portal Vein Pressure ◽  
Wedged Hepatic Vein Pressure

scholarly journals COMPARISON OF WEDGED HEPATIC VEIN PRESSURE WITH PORTAL VEIN PRESSURE IN HUMAN SUBJECTS WITH CIRRHOSIS 12

1955 ◽  
Vol 34 (2) ◽  
pp. 213-218 ◽  
Author(s):  
Telfer B. Reynolds ◽  
Donald C. Balfour ◽  
David C. Levinson ◽  
William P. Mikkelsen ◽  
Arthur C. Pattison
Keyword(s):  
Portal Vein ◽  
Hepatic Vein ◽  
Human Subjects ◽  
Portal Vein Pressure ◽  
Wedged Hepatic Vein Pressure

scholarly journals Portal vein thrombosis in cirrhotic patients - it is always the small pieces that make the big picture

2018 ◽  
Vol 24 (39) ◽  
pp. 4419-4427 ◽  
Author(s):  
Irina Gîrleanu ◽  
Anca Trifan ◽  
Carol Stanciu ◽  
Cătălin Sfarti
Keyword(s):  
Portal Vein ◽  
Portal Vein Thrombosis ◽  
Vein Thrombosis ◽  
Big Picture ◽  
Cirrhotic Patients

scholarly journals Doppler ultrasound in liver cirrhosis: correlation of hepatic artery and portal vein measurements with model for end-stage liver disease score in Egypt

2020 ◽  
Vol 51 (1) ◽  
Author(s):  
Ahmed Abdelrahman Mohamed Baz ◽  
Rana Magdy Mohamed ◽  
Khaled Helmy El-kaffas
Keyword(s):  
Liver Cirrhosis ◽  
Liver Disease ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Meld Score ◽  
Hepatic Decompensation ◽  
End Stage Liver Disease ◽  
Cirrhotic Patients ◽  
Us Findings ◽  
End Stage

Abstract Background Liver cirrhosis is a multi-etiological entity that alters the hepatic functions and vascularity by varying grades. Hereby, a cross-sectional study enrolling 100 cirrhotic patients (51 males and 49 females), who were diagnosed clinically and assessed by model for end-stage liver disease (MELD) score, then correlated to the hepatic Doppler parameters and ultrasound (US) findings of hepatic decompensation like ascites and splenomegaly. Results By Doppler and US, splenomegaly was evident in 49% of patients, while ascites was present in 44% of them. Increased hepatic artery velocity (HAV) was found in70% of cases, while 59% showed reduced portal vein velocity (PVV). There was a statistically significant correlation between HAV and MELD score (ρ = 0.000), but no significant correlation with either hepatic artery resistivity index (HARI) (ρ = 0.675) or PVV (ρ =0.266). Moreover, HAV had been correlated to splenomegaly (ρ = 0.000), whereas HARI (ρ = 0.137) and PVV (ρ = 0.241) did not significantly correlate. Also, ascites had correlated significantly to MELD score and HAV (ρ = 0.000), but neither HARI (ρ = 0.607) nor PVV (ρ = 0.143) was significantly correlated. Our results showed that HAV > 145 cm/s could confidently predict a high MELD score with 62.50% and 97.62 % sensitivity and specificity. Conclusion Doppler parameters of hepatic vessels (specifically HAV) in addition to the US findings of hepatic decompensation proved to be a non-invasive and cost-effective imaging tool for severity assessment in cirrhotic patients (scored by MELD); they could be used as additional prognostic parameters for improving the available treatment options and outcomes.

Metabolic effects of oral fructose in the liver of fasted rats

1984 ◽  
Vol 247 (4) ◽  
pp. E505-E512 ◽  
Author(s):  
C. B. Niewoehner ◽  
D. P. Gilboe ◽  
G. A. Nuttall ◽  
F. Q. Nuttall
Keyword(s):  
Uric Acid ◽  
Portal Vein ◽  
Hepatic Vein ◽  
Glycogen Synthase ◽  
Control Level ◽  
Liver Glycogen ◽  
Glycogen Storage ◽  
Metabolic Effects ◽  
Serum Triglycerides ◽  
Fasted Rats

Twenty-four-hour-fasted rats were given fructose (4 g/kg) by gavage. Fructose absorption and the portal vein, aorta, and hepatic vein plasma fructose, glucose, lactate, and insulin concentrations as well as liver fructose and fructose 1-P, glucose, glucose 6-P, UDPglucose, lactate, pyruvate, ATP, ADP, AMP, inorganic phosphate (Pi), cAMP, and Mg2+, and glycogen synthase I and phosphorylase alpha were measured at 10, 20, 30, 40, 60 and 120 min after gavage. Liver and muscle glycogen and serum uric acid and triglycerides also were measured. Fifty-nine percent of the fructose was absorbed in 2 h. There were modest increases in plasma and hepatic fructose, glucose, and lactate and in plasma insulin. Concentrations in the portal vein, aorta, and hepatic vein plasma indicate rapid removal of fructose and lactate by the liver and a modest increase in production of glucose. The source of the increase in plasma lactate is uncertain. Hepatic glucose 6-P increased twofold; UDPglucose rose transiently and then decreased below the control level. Fructose 1-P increased linearly to a concentration of 3.3 mumol/g wet wt by 120 min. There was no change in ATP, ADP, AMP, cAMP, Pi, or Mg2+. Serum triglycerides and uric acid were unchanged. Glycogen synthase was activated by 20 min without a change in phosphorylase alpha. This occurred with a fructose dose that did not significantly increase either the liver glucose or fructose concentrations. Liver glycogen increased linearly after 20 min, and glycogen storage was equal in liver (38.4%) and muscle (36.5%).(ABSTRACT TRUNCATED AT 250 WORDS)

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